کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
6087542 1589429 2014 10 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Serum from patients with systemic vasculitis induces alternatively activated macrophage M2c polarization
موضوعات مرتبط
علوم زیستی و بیوفناوری ایمنی شناسی و میکروب شناسی ایمونولوژی
پیش نمایش صفحه اول مقاله
Serum from patients with systemic vasculitis induces alternatively activated macrophage M2c polarization
چکیده انگلیسی


- A robust method for studies of macrophage polarization has been developed.
- Serum from AAV patients promotes a M2c macrophage polarization.
- Serum induced M2c macrophages express high levels of MerTK.
- M2c macrophages phagocyte apoptotic material better than other macrophage subtypes.
- GPA patients in remission are more immunologically active than MPA patients.

Anti-neutrophil cytoplasmic antibody associated vasculitides (AAV) are conditions defined by an autoimmune small vessel inflammation. Dying neutrophils are found around the inflamed vessels and the balance between infiltrating neutrophils and macrophages is important to prevent autoimmunity. Here we investigate how sera from AAV patients may regulate macrophage polarization and function. Macrophages from healthy individuals were differentiated into M0, M1, M2a, M2b or M2c macrophages using a standardized protocol, and phenotyped according to their expression surface markers and cytokine production. These phenotypes were compared with those of macrophages stimulated with serum from AAV patients or healthy controls. While the healthy control sera induced a M0 macrophage, AAV serum promoted polarization towards the M2c subtype. No sera induced M1, M2a or M2b macrophages. The M2c subtype showed increased phagocytosis capacity compared with the other subtypes. The M2c polarization found in AAV is consistent with previous reports of increased levels of M2c-associated cytokines.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Clinical Immunology - Volume 152, Issues 1–2, May–June 2014, Pages 10-19
نویسندگان
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